“Dopamine has been demonstrated to play a role in pain processing in multiple levels of the central nervous system including the spinal cord,[46] periaqueductal gray (PAG),[47] thalamus,[48] basal ganglia,[49][50] insular cortex,[51][52] and cingulate cortex.[53] Accordingly, decreased levels of dopamine have been associated with painful symptoms that frequently occur in Parkinson’s disease.[54] Abnormalities in dopaminergic neurotransmission have also been demonstrated in painful clinical conditions, including burning mouth syndrome,[55] fibromyalgia,[56][57] and restless legs syndrome.[58] In general, the analgesic capacity of dopamine occurs as a result of dopamine D2 receptor activation; however, exceptions to this exist in the PAG, in which dopamine D1 receptor activation attenuates pain presumably via activation of neurons involved in descending inhibition.[59] In addition, D1 receptor activation in the insular cortex appears to attenuate subsequent pain-related behavior.”https://en.wikipedia.org/wiki/Dopamine